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inducing antigen in EAE is known, whereas the putative antigen in MS is not Also incorporated into most theories of the immune pathogenesis is an alteration of the blood-brain barrier, represented by adhesion of lymphocytes to endothelial cells Whether this is an active interaction or a passive event triggered by antigenic attraction is not clear; nonetheless, these cell-vascular interactions have been incorporated into pathogenic theories and is the basis of newer treatments for MS As matters now stand, the focus of attention is on the pathogenic role of speci c subsets of T lymphocytes, which regulate humoral immune responses either as potentiators (T-helper cells) or as inhibitors (T-suppressor cells) of immunoglobulin production by the B lymphocytes So-called helper (CD41) T cells are found in abundance within MS plaques and surrounding venules (perivascular cuf ng) It has been demonstrated that T-cell receptors respond to antigens presented by (major histocompatibility complex, or MHC) class II molecules on macrophages and astrocytes This interaction is thought to stimulate T-cell proliferation and a cascade of related cellular events, including the activation of B cells and macrophages and the secretion of cytokines (one of which is IFN- and another IFN- ; see further on) These cellular events are accompanied by a breakdown of the blood-brain barrier and, if suf ciently intense, by destruction of myelin (see review by French-Constant) A reduction in T cells, both helper and suppressor subsets, or an increase in the ratio of helper-suppressor cells, may precede an acute attack and appears to be associated with increasing disability in patients with MS Always in the background is the element of genetic susceptibility, presumably making certain individuals prone to these immunologic events The foregoing data notwithstanding, it must be added that the immune mechanisms in MS are not fully speci ed and the autoimmune hypothesis is not beyond challenge It is noteworthy that the prevalence of other diseases of presumed autoimmune origin is no higher in MS patients than in the general population (De Keyser) Moreover, the course of MS has been altered only inconsistently by the administration of any of the nonspeci c immunosuppressive therapies (Goodkin et al, 1992) Also worthy of comment is the relatively ineffective remyelination of the MS plaque When remyelination of denuded axons occurs, thinly myelinated bers are produced, creating areas of socalled shadow plaques Histologic evidence suggests that some of the oligodendrocytes are destroyed in areas of active demyelination but also that some of the remaining ones have little ability to proliferate Instead, there is an in ux of oligodendroglial precursor cells, which mature into oligodendrocytes and provide the remaining axons with new myelin Probably the astrocytic hyperplasia in regions of damage and the persistent in ammatory response account for some of the inadequacy of the reparative process (see Prineas et al).

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points about the pathophysiology of demyelination When the demyelinative process is acute and reversible within a few days, the block in nerve ber conduction is obviously physiologic rather than pathologic; in such a brief period, recovery is unlikely to have been due to remyelination Probably recovery is due to subsidence of the edema and acute in ammatory changes in and around the lesion Remyelination probably does occur, as described above, but it is a slower process and partial at best, and its functional effects in the CNS are possibly expressed as a slowing of nerve conduction, which, if present in an eye with normal vision, may account for the reduction in icker fusion and in the perception of multiple visual stimuli (Halliday and McDonald) It also explains one of the classic symptoms of optic neuritis a reduction in the intensity (desaturation) of the color red It is clear, however, that many of the plaques visualized on MRI are unaccompanied by corresponding symptoms; in some cases, there is no electrophysiologic abnormality as tested with evoked responses Either there has been complete remyelination in these plaques, suf cient to support clinical functioning, or, in the acute stage, the plaque may represent edema rather than demyelination Another classic feature of MS is the temporary induction, by heat or exercise, of symptoms such as unilateral visual blurring (the Uhthoff phenomenon) or tingling and weakness of a limb (the basis of the hot-tub test used in previous years) This has been shown experimentally to represent an extreme sensitivity of conduction in demyelinated nerve bers to an elevation in temperature A rise of only 05 C (09 F) can block electrical transmission in thinly myelinated or demyelinated bers Likewise, hyperventilation slows conduction of the visual evoked response, an effect that is rarely perceived by the patient The remarkable sensitivity of demyelinated and remyelinated regions to subtle metabolic and environmental changes provides an explanation for the rapid onset of symptoms in some patients and the apparent uctuations of MS that show no laboratory evidence of active in ammatory changes in the CNS Smoking, fatigue, hyperventilation, and a rise in environmental temperature are all capable of brie y worsening neurologic functioning and are easily confused with relapses of disease.

A variety of events occurring immediately before the initial symptoms or exacerbations of MS have been invoked as precipitating factors The most common are infection, trauma, and pregnancy However, in our view, none of these has been convincingly related to an increased risk of new attacks of MS, and there are no adequately controlled studies that would contradict this view Nonetheless, we have had experience with several patients who regularly had acute exacerbations of MS following each outbreak of labial genital herpes The incidence of respiratory or gastrointestinal viral infections that precede the onset or exacerbations of the disease varies greatly in different series, from 5 to 50 percent The swine in uenza vaccine, which was given to 45 million persons in the United States in late 1976, caused a slight increase in the incidence of Guillain-Barre disease but not of MS (Kurland et al), and more recent surveys of immunization programs, such as the one by Confavreux and colleagues (2001), con rm this The possible role of trauma in precipitating MS is more dif cult to assess McAlpine and Compston found that the incidence of trauma within a 3-month period preceding the onset of MS was slightly greater than in a random control group of hospital patients